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8/10/2019 [2003]Dissection of the Aorta a New Approach
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VIEWPOINT
Dissection of the aorta: a new approachM Mikich. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Heart2003;89:68
There are two generally proposed causes of dissectionof the aorta: (1) cleavage caused by blood entering thetear; and (2) haemorrhage that dissects the media andtear secondary to the cleavage. Using analysis ofpressures and forces, this article shows that, on someoccasions, these mechanisms alone cannot beresponsible for causing aortic dissection. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
This article addresses a possible cause ofdissection of the aorta. Let us start with a
variation of dissection which is not socommonthat is,the dissection that has an entrytear located just beyond the left subclavian artery,but which extends proximally into the ascendingaorta (in other words, the dissection cleavagepropagates from the tear towards the aorticroot).1 2
To simplify matters,let us assume that the bodyis in the supine position. In other positions of thebody the calculation is a bit more complicated butthe result is the same.
ANALYSIS OF PRESSURES AND FORCESForces acting on the flap proximally fromthe tearIt is thought that cleavage from blood entering
through the tear causes the propagation of
dissection towards the aortic root. This is repre-
sented in fig 1. Points denoted with F are in the
false channel and those denoted as T are in the
true channel. If we compare pressure in the true
channel at the tear to pressure at the aortic root it
is obvious that pressure in the true channel
always gradually rises from the tear to the aortic
root (so pressure at T1 is greater than pressure at
the tear, pressure at T2 is greater than pressure at
T1, and pressure at T3 is greater than at T2).
If there is no flow in the false channel the pres-sure at any point within the false channel must bethe same as the pressure at the tear (so pressure
at F0, F1, F2, and F3 is the same as at the tear).
When applying these facts to fig 1 it is obviousthat pressure at point T1 is greater than the pres-
sure at point F1, that pressure at T2 is greater than
pressure at F2, and that pressure at T3 is greaterthan pressure at F3. This means that the pressure
difference pushes the flap towards the adventitia.
Therefore, cleavage by blood from the tear cannotbe the cause of propagation of dissection from the
tear towards the aortic root. This is true no matter
how close the tear is to the aortic root. Even if the
tear is just above the aortic root (as in type I) it isobvious that the cleavage caused by blood from
the tear cannot undermine the aortic valve.
If blood enters from the true channel throughthe tear into the false channel (that is, flows
towards point F3) then pressure at F1 is lower
than pressure at the tear (because liquid can flow
only from higher pressure towards lower pres-
sure), pressure at F2 is lower than at F1, and
pressure at F3 is lower than at F2. Therefore, the
pressure difference that pushes the flap towards
the adventitia is greater than in the case in which
there is no flow in the false channel.
Pressure drop in the aortaTo calculate maximum forces acting on the flap,
the maximum pressure difference between a
point in the false channel and its most adjacentpoint in the true channel (for instance, between
the points F0 and T0) must be determined. The
maximum pressure difference is when there is
maximum pressure drop along the aorta. Since
the maximum pressure at the aortic root is systo-
lic and minimum pressure at the distal end of the
aorta is diastolic, the maximum pressure differ-
ence between the aortic root and distal end
cannot be greater than systolic pressure minus
diastolic pressure. It can also be assumed that
pressure linearly falls from the aortic root to the
distal end.
So if, for example, systolic pressure is
135 mm Hg, diastolic pressure is 90 mm Hg, andthe length of the aorta is 45 cm, then the
maximum pressure drop is (135 90)/45 =1 mm Hg/cm (this pressure drop will be used in
further calculations).
Forces acting on the flap distally from tearIf the distance between the tear and T0 (fig 1) is
1 cm then pressure at T0 is 1 mm Hg lower than
at the tear. When there is no flow in the false
Figure 1 Calculation of forces that act on the flap.Point F0 is just at the distal end of the dissection.
. . . . . . . . . . . . . . . . . . . . . . .
Correspondence to:Mr Boris Mikich, FranaAlfirevica 29, 10000Zagreb, Croatia;[email protected]. . . . . . . . . . . . . . . . . . . . . . .
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channel, the pressure at F0 (point F0 is just at the distal endof the false channel) is equal to the pressure at the tear, so the
pressure at F0 is 1 mm Hg higher than at T0. Since the
pressure difference at the beginning of the flap (just at the
tear) is zero, the mean pressure difference on the flap distally
from the tear is (0 + 1)/2 = 0.5 mm Hg. If we suppose, for the
purpose of this discussion, that the transverse length of the
flap is 5 cm (longitudinal length is equal to distance between
tear and F0 or T0that is, 1 cm) then the area of the flap dis-
tal to the tear is 5 1 cm2which, when multiplied by the meanpressure difference on the flap, gives a force by which the flap
distal to the tear is pushed towards the true channel.
Converting 0.5 mm Hg to N/m2 gives (1 mmHg = 132.88
N/m2 at 20C): 0.5 132.88 = 66.4 N/m2, and converting cen-
timetres to metres 1 cm = 0.01 m and 5 cm = 0.05 m. Thus,the force is:
66.4 0.01 0.05 = 0.0332 N.
This force is too small to cause any further increase of the
dissection in the distal direction. If blood enters the false
channel then the pressure at F0 is lower than in the case when
there is no flow in the false channel, therefore forces on the
flap are lower too.
Forces from haemorrhageIt is also thought that haemorrhage dissects the media and
that tear is secondary to it. Figure 2 shows a haemorrhage in
the media. Point T is the point in the lumen of the aorta whichis nearest to the haematoma. For the purpose of this
discussion, let us say that the haemorrhage is situated just
beyond the left subclavian artery, about 15 cm from the aortic
root. If we use the same pressure drop as in the previous
example, then pressure at point T is 15 cm 1 mm Hg/cm =15 mm Hg lower than at the aortic root. The maximum possi-
ble pressure in the haematoma is pressure at the aortic root.
This means that pressure in the haematoma cannot be more
than 15 mm Hg higher than at point T and from that the
maximum force produced by the pressure difference between
the haematoma and point T can be calculated.
Let us suppose that the haematoma has an area of 2 2 mm.Converting 15 mm Hg to N/m2 gives: 15 132.88 = 1993 N/m2,
and converting millimetres to metres, 2 mm = 0.002 m. Thus,the maximum force that is produced by the pressure
difference between the haematoma and T is:
1993 0.002 0.002 = 0.00797 N.
That force is too small to make any cleavage in the media orto tear the intima. If there is haemorrhage at the aortic root
then the pressure difference between the haematoma and the
most adjacent point to it in the lumen of the aorta is zero;
therefore it is obvious that there is no force at all and that
blood from that haematoma cannot undermine the aortic
valve.
THE REAL CAUSE OF DISSECTIONFormation of the dissectionIf the aortic smooth muscles contract the adventitia will
follow that contraction. But as seen in fig 3, at the area of the
aorta where the left subclavian, left carotid, and brachio-
cephalic artery originate, downward movement of the aortic
wall is very limited by those arteries. Upward movement of
area A of the aorta is very limited by area D of the aorta. So at
the segment of the aorta which comprises the origin of the left
subclavian artery and area A, the aortic wall is fixed at the
upper and the lower part, so at the upper and lower part of the
segment the adventitia can only partially follow the contrac-
tion of smooth muscles (fig 4). As a consequence high stresses
Figure 2 Calculation of forces that act from the haemorrhage inthe media
Figure 3 Limitation of upwardmovement of area A by area D.
Figure 4 Forces Fs from smooth muscles cause stresses in themedia.
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develop in the media in that segment. If too strong a contrac-
tion of smooth muscles (spasm) occurs, dissection of the
media will take place, especially if there are areas of cystic
degeneration in the media and/or if there is any other
weakness in the media.
Why does dissection take place just beyond the origin of the
left subclavian artery and not at area A? It is because the
smooth muscles of the aorta (and thus also forces from the
smooth muscles) are not arranged around the originof the left
subclavian artery as evenly as they are at area A. This uneven
distribution causes the concentration of forces in the aortic
media at the origin of the left subclavian artery which then
causes dissection.
Eventually, if the forces from the smooth muscles continue
to increase, the intima and part of the media on the smooth
muscle will break and a tear will result.
Propagation of dissectionFigure 5 shows a transverse cross section of dissection through
the flap. It can be seen that blood pressure forces act on all the
inside surfaces of the false and true channels. Assuming, for
simplicitys sake, that pressures both in the true and in the
false channel are the same, the forces acting on the flap from
the false channel and from the true channel are also equal(and so cancel each other) and therefore they are not shown.
The forces shown stretch the aortic wall. While stretching,
the aortic wall stretches the flap in the direction that is
perpendicular to the long axis of the aorta and parallel with
the flap. Because each force must have a counter force of the
same intensity and opposite direction it means that the flap
pulls the aortic wall by force Ff (fig 5, right). That force is
caused by elasticity of the flap and/or the presence of forces
from smooth muscles in the flap. This force Ff by which the
flap pulls the aortic wall tends to damage the media further
and to increase dissection in the transverse direction. The
increasing dissection in the transverse direction is accompa-
nied by movement of the flap towards the centre of the aorta.
This movement pulls the rest of the flap which is located dis-tally and/or proximally from the part of the flap shown in cross
section, and that causes further dissection in the distal and/or
proximal direction.
If blood pressure rises the stretching of the flap increases;
consequently the forces that tend to damage the media and to
increase dissection also rise. Once the flap, which is
perpendicular to the long axis of the aorta, reaches a certain
length (the length depending on pressure in the aorta), the
elastic forces from the flap alone are sufficient to increase dis-
section further.
If a tear does not occur, blood from haemorrhage could
slowly fill the false channel, thus establishing in the false
channel the same pressure as in the aorta, as occurs when
there is a tear. But, because of low inflow of blood from haem-orrhage in this case, dissection can propagate only very slowly.
CONCLUSIONDissection takes place as a consequence of major contraction
of the smooth muscles, especially when there are areas of
cystic degeneration in the media, and haemorrhage takes
place because of dissection of the media. Administration ofblockers and/or calcium antagonists will reduce this strong
contraction of the smooth muscles, thus reducing dissection.3
On the other hand, discontinuation of long term therapy with
blockers may provoke dissection.4
Fibrous tissue at the aortic root also fixes the aortic wall,
which makes this part of the aorta also suitable for initiating
dissection. This fixing of the aortic wall explains why morethan 95% of dissections begin at two places: either just above
the aortic valve or just beyond the origin of the left subclavian
artery.5
In hypertensives there is an increase in smooth muscle
mass and that also produces a stronger force.6 7 That, together
with acquired cystic degeneration in hypertensives, mayexplain why dissection takes place mostly in hypertensives.
Smooth muscles in the media in large, elastic arteries are
generally helically oriented.8 Therefore it is readily possiblethat dissection propagates in a direction perpendicular to the
orientation of these helically oriented smooth muscles
(analogous to normal propagation which is perpendicular tocircumferentially oriented smooth muscles). As a result spiral
dissection develops, known as spiral barber pole dissection.1
REFERENCES1 Schlant RC, Alexander RW.Hursts the heart, 8th edn. New York:
McGraw-Hill, 1994:2170.2 Hurst JW, Alpert JS.Diagnostic atlas of the heart. New York: Raven
Press, 1994:337.3 Hoshino T, Ohmae M, Sakai A. Spontaneous resolution of a dissection
of the descending aorta after medical treatment with a beta blocker anda calcium antagonist.Br Heart J1987;58:824.
4 Eber B, Tscheliessnigg KH, Anelli-Monti M,et al.Aortic dissection due todiscontinuation of beta-blocker therapy.Cardiology1993;83:12831.
5 Hurst JW, Alpert JS.Diagnostic atlas of the heart. New York: RavenPress, 1994:338.
6 Owens GK, Schwartz SM. Alterations in vascular smooth muscle mass inthe spontanteneously hypertensive rat. Role in cellular hypertrophy,hyperploidy and hyperplasia.Circ Res1982;51:2809.
7 Owens GK, Schwartz SM. Vascular smooth muscle cell hypertrophy andhyperploidy in the Goldblatt hypertensive rat. Circ Res1983;53:491501.
8 Schlant RC,Alexander RW. Hursts the heart, 8th ed. New York:McGraw-Hill, 1994:31.
Figure 5 Transverse (perpendicular to the long axis of the aorta)cross section of a dissection. The left and right cross sections areidentical, but in the right cross section the flap is not present so thatforces Ff can be shown. Forces from blood pressure acting on theflap from the false channel and the true channel are equal andcancel each other, and therefore they are not shown. Fp, forces fromblood pressure in the aorta; Ff, forces with which the flap pulls theaortic wall.
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